Skip to main content
. 2018 Jul 10;33:105–121. doi: 10.1016/j.ebiom.2018.07.002

Fig. 4.

Fig. 4

BMAL1- and HKDC1-KD leads to metabolic changes in SW480 and SW620 cells and altered drug response.

(a) Energy map of SW480 (upper panel) and SW620 (lower panel) control and shBMAL1 cells untreated or after treatment with WZB117 or oxaliplatin. The mean of three treatment timepoints after synchronization is shown (18 h, 21 h, 24 h). Mean ± SEM, n = 16. (b) Glycolysis of SW480 (left panel) and SW620 (right panel) control, shBMAL1 and shHKDC1 cells at different timepoints after synchronization. Cells were either untreated or treated with WZB117. Mean ± SEM, n = 5. (c) Glycolytic capacity of SW480 (left panel) and SW620 (right panel) control, shBMAL1 and shHKDC1 cells treated at three different timepoints after synchronization (18 h, 21 h, 24 h). Cells were either untreated or treated with WZB117. Mean ± SEM, n = 5. (d) Basal respiration of SW480 (upper panel) and SW620 (lower panel) control, shBMAL1 and shHKDC1 cells treated at three different timepoints after synchronization (18 h, 21 h, 24 h). Cells were either untreated or treated with WZB117. Mean ± SEM, n = 5. (e) Maximum respiration of SW480 (upper panel) and SW620 (lower panel) control, shBMAL1 and shHKDC1 cells synchronized at different timepoints. Cells were either untreated or treated with WZB117. Mean ± SEM, n = 5. (f) ATP production of SW480 (upper panel) and SW620 (lower panel) control, shBMAL1 and shHKDC1 cells synchronized at different timepoints. Cells were either untreated or treated with WZB117. Mean ± SEM, n = 5. * = p < .05, ** = p < .01, *** = p < .001. For more data, see also Supplementary Fig. 5.